Overview
Why Bilirubin Rises—and Why the Brain Matters
Newborn bilirubin is produced mainly when fetal red blood cells are broken down.
Newborn bilirubin is produced mainly when fetal red blood cells are broken down. Neonates have a relatively large red-cell mass, shorter red-cell survival, and an immature hepatic conjugation system, so unconjugated bilirubin can accumulate during the first days of life. Unconjugated bilirubin is lipid-soluble. It circulates largely bound to albumin and normally reaches the liver, where glucuronidation makes it easier to excrete. When the bilirubin load rises, albumin binding is reduced, or illness disrupts the blood–brain barrier, unbound bilirubin can enter brain tissue. Acute bilirubin encephalopathy may begin with irritability, a high-pitched cry, or abnormal tone and can progress to seizures, coma, or death. The visible yellow colour is therefore only a clue; neurological status and a measured bilirubin value determine urgency. Phototherapy changes the chemistry of unconjugated bilirubin in the skin and subcutaneous tissue. Narrow-spectrum blue-green light converts the native 4Z,15Z bilirubin into water-soluble configurational isomers, lumirubin, and photo-oxidation products. Lumirubin is essentially irreversible and is the predominant excreted photoisomer. These products can leave through bile and urine without first requiring hepatic glucuronidation, which is why phototherapy works even...
